Adenoid cystic carcinoma (ACC) of the palate is a malignant salivary gland neoplasm typically characterized by perineural invasion, recurrent MYB-NFIB fusion, and an indolent clinical course. We report an atypical case of palatal ACC arising during pregnancy that exhibited rapid progression, upregulated estrogen receptor (ER) expression, and atypical histopathology. ACC most frequently involves the parotid and palatal glands and is histologically stratified into cribriform, tubular, and solid subtypes, with solid pattern carrying the poorest prognosis. The tumor is characteristically indolent yet relentless, with a marked propensity for perineural invasion, which often manifesting as pain, facial paralysis, or lingual numbness and a preference for hematogenous over lymphatic spread, with lungs as the most common site of distant metastasis. Wide local excision remains the cornerstone of treatment. The patient first presented in early pregnancy with focal microvascular congestion and pain of the palatal mucosa. Within 24 weeks, the lesion progressed to full-thickness perforation of the palatal mucosa and underlying bone. After delivery by cesarean section at 37 weeks of gestation and hospital admission, imaging revealed bilateral cervical lymph node involvement and bilateral pulmonary metastases, a trajectory that diverges sharply from the slow-growing course typical of ACC. Immunohistochemistry demonstrated small cribriform architecture with patchy or absent expression of conventional myoepithelial markers. Fluorescence in situ hybridization (FISH) confirmed an MYB-NFIB fusion, the hallmark molecular alteration of ACC, anchoring the diagnosis despite the unusual phenotype. Notably, ER expression was upregulated in tumor tissue, suggesting that gestational hormonal shifts may have modulated tumor progression; however, the marked nuclear atypia, high proliferative index, and early nodal and pulmonary metastasis were more consistent with intrinsic high-grade transformation of ACC. After integrating clinical, biological, molecular, and genotypic findings and excluding morphological mimics, the final diagnosis was atypical ACC of the palate. This case underscores the need for heightened clinical vigilance toward focal palatal microvascular congestion during pregnancy, which may herald an aggressive oral malignancy in this hormonally distinct population. Early recognition, supplemented by molecular confirmation (MYB-NFIB FISH) when histology is equivocal, is essential for timely intervention and improved outcomes in atypical, pregnancy-associated ACC of the oral and maxillofacial region.

To describe the diagnostic challenges, treatment response, and potential benefits and risks of cytoreductive surgery in de novo metastatic prostatic small cell neuroendocrine carcinoma (SCNEC).

We retrospectively reviewed the clinical course of one patient with de novo metastatic prostatic SCNEC.

A 50-year-old man presented in June 2022 with progressive dysuria for more than 1 year and acute urinary retention for 1 day. Transurethral resection of the prostate (TURP) was performed to relieve obstruction, and review of the specimen supported SCNEC. Staging ¹⁸F-FDG PET/CT showed an FDG-avid prostate, multiple lymph nodes, and bilateral non-FDG-avid pulmonary nodules without a dominant pulmonary primary; a prostatic primary with clinically suspected pulmonary metastases was favored, although the lung lesions were not biopsied. Seven cycles of etoposide plus cisplatin (EP) produced marked local regression, including a reduction in prostate volume from 72 to 17 cm³, but residual tumor persisted and a RECIST response category could not be assigned retrospectively. Cytoreductive laparoscopic radical prostatectomy was performed in February 2023. Postoperative pathology showed a mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN). A vesicourethral anastomotic leak improved conservatively, and urinary obstruction improved for approximately 3 months. Disease progressed in July 2023, and irinotecan plus carboplatin provided no durable clinical disease control. The patient died in December 2023, approximately 18 months after diagnosis.

EP can produce substantial but temporary regression in metastatic prostatic SCNEC. This case did not establish a survival benefit from surgery, although temporary relief of urinary obstruction was reported. Systemic therapy should remain the priority, and surgery should be limited to carefully selected local-control or palliative indications.

Poroid hidradenoma (PH) is an infrequently encountered benign adnexal neoplasm exhibiting eccrine differentiation. Histopathologically, PH displays a distinctive combination of hidradenoma-like architectural organization characterized by a purely intradermal localization with both solid and cystic components, and cytological attributes of poroid neoplasms, consisting predominantly of poroid and cuticular cells. In the present report, we document a case of pigmented PH arising on the thigh of a 44-year-old male patient and discuss its characteristics and clinical course.

N ⁶-methyladenosine (m⁶A) regulates nearly every aspect of messenger RNA (mRNA) processing and function, impacting downstream gene expression programs. Changes in m⁶A have been implicated in many different types of cancer, and inhibition of m⁶A installation is emerging as a cancer therapeutic strategy. However, chemoresistance remains a significant clinical challenge in the treatment of glioblastoma (GBM). We established GBM cell culture models of acquired temozolomide (TMZ) resistance, analyzed the role of m⁶A in controlling resistance-associated pathways, and assessed the effects of METTL3 inhibition. We show that m⁶A stabilizes key genes and pathways promoting TMZ resistance, and that METTL3 inhibition can reverse this and restore TMZ sensitivity. These findings highlight that TMZ resistance can occur independent of a glioma stem cell population and that changes in m⁶A need not be driven by changes in METTL3 expression. Collectively, our results suggest that genes associated with TMZ resistance are stabilized by m⁶A methylation even as the majority of the transcriptome remains subject to m⁶A-mediated mRNA decay. Moreover, these data highlight METTL3 inhibition as a promising therapeutic approach to overcoming TMZ resistance in GBM.

Glioma, the most prevalent and aggressive primary malignant brain tumor, is associated with poor clinical outcomes. There is an urgent need for novel biomarkers to predict survival and therapeutic response, as existing markers offer limited prognostic utility.

Single-cell RNA sequencing data from glioma patients were analyzed to identify CD8+ T cell-related genes. Four machine learning algorithms (XGBoost, Gradient Boosting Machine, LASSO, and Random Forest) were employed to screen genes associated with glioma prognosis. The expression of HIST1H2BJ was detected in clinical samples. Flow cytometry was performed to assess cell apoptosis, while Transwell assays were conducted to evaluate cell invasion and migration capabilities, respectively. A novel prognostic model, the Immune and Metabolic Prognostic Model of Glioma (IMPMG), was developed, and its accuracy was evaluated using receiver operating characteristic (ROC) curves and decision curve analysis (DCA). Additionally, potential small-molecule compounds were screened via molecular docking, and the binding stability was evaluated by molecular dynamics (MD) simulations.

HIST1H2BJ was identified as a critical gene associated with glioma prognosis. Functional assays confirmed that HIST1H2BJ knockdown promoted cell apoptosis and inhibited cell invasion and migration. Glioma patients with high HIST1H2BJ expression were closely associated with an immunosuppressive tumor microenvironment, with significantly increased infiltration of M2 macrophages and regulatory T cells (Tregs), as well as upregulated immune checkpoint expression. The IMPMG model, integrating HIST1H2BJ, immune-metabolic genes, and clinical variables, demonstrated superior prognostic accuracy (AUC > 0.86) and clinical utility compared to existing models. Furthermore, molecular docking identified VX-680 and A.770041 as candidate compounds associated with HIST1H2BJ-high drug-sensitivity prediction; their direct binding to HIST1H2BJ was assessed only in silico by molecular docking and dynamics simulations and requires experimental validation.

This study establishes HIST1H2BJ as an independent prognostic factor for glioma patient survival and a candidate prognostic biomarker whose therapeutic relevance requires further functional and preclinical investigation.

Insulin-like growth factor binding protein 1 (IGFBP1) is documented as a pro- tumorigenic gene in various cancers; nevertheless, its specific function in esophageal carcinoma (ESCA) is unclear. This study used data obtained from The Cancer Genome Atlas (TCGA) to assess IGFBP1 expression, investigating its clinical outcome-related relevance, and explore its correlation in the context of ESCA tumor microenvironment. The Wilcoxon rank-sum test indicated a notable overexpression of IGFBP1 in ESCA compared to normal tissues, which was further validated via immunohistochemistry. Functional enrichment analysis identified tumor-related pathways, while ssGSEA/CIBERSORT methods linked IGFBP1 expression to altered immune infiltration. Furthermore, an investigation of single-cell data sourced from the GSE196756 data uncovered unique immune cell subsets linked to the expression of IGFBP1. The application of Cox regression alongside Kaplan-Meier survival analyses indicated that elevated levels of IGFBP1 were correlated with unfavorable outcomes in overall survival (OS), and disease-specific survival (DSS). Functional validation utilizing CCK-8 and transwell assays revealed that IGFBP1 silencing significantly suppressed the proliferative, invasive, and migratory capabilities of ESCA cell lines. Furthermore, in vivo analyses also presented similar results. Collectively, these results position IGFBP1 as a prognostic biomarker in ESCA, highlighting its functional involvement in tumor progression.

Accurate pre-operative assessment of surgical difficulty and post-operative risk in rectal cancer remains challenging. Conventional indices such as body mass index (BMI) fail to adequately reflect the pelvic surgical anatomy due to their systemic nature. Mesorectal fat volume-an imaging-derived, site-specific parameter-may better represent the operative field and associated risks, while also serving as a marker of regional adiposity relevant to nutritional and metabolic status.

This single-center retrospective cohort study (2018-2026) analyzed 450 consecutive patients undergoing elective rectal cancer surgery with total mesorectal excision. Mesorectal fat volume was quantified using pre-operative computed tomography or magnetic resonance imaging with semi-automated segmentation. Patients were categorized into quartiles based on mesorectal fat volume. Operative outcomes and 30-day post-operative complications were compared across quartiles. Multivariable linear and logistic regression analyses were performed to identify independent predictors. Receiver operating characteristic (ROC) curve analysis was used to evaluate the discriminative performance of mesorectal fat volume, BMI, and pelvic index.

A total of 450 patients were stratified into quartiles according to mesorectal fat volume (MFV). Patients in the highest MFV quartile had significantly longer operative times (182.26 ± 9.28 vs. 163.03 ± 9.67 min, P < 0.001), greater intraoperative blood loss (169.63 ± 39.00 vs. 94.55 ± 40.08 mL, P < 0.001), higher conversion-to-open surgery rates (27.68% vs. 5.17%, P < 0.001), and higher 30-day post-operative complication rates (63.39% vs. 29.31%, P < 0.001) than those in the lowest MFV quartile. In multivariable analyses, MFV remained an independent predictor of post-operative complications (OR = 1.37, 95% CI: 1.21-1.55, P < 0.001), whereas BMI and pelvic index were not independently associated with complications. The multivariable prediction model demonstrated moderate discriminative ability (AUC = 0.683). Among the individual anthropometric measures, MFV demonstrated moderate discriminative ability (AUC = 0.655; 95% CI, 0.605-0.705), outperforming BMI (AUC = 0.552; 95% CI, 0.499-0.606) and pelvic index (AUC = 0.468; 95% CI, 0.415-0.522).

CT-derived mesorectal fat volume is independently associated with increased operative difficulty and a higher risk of post-operative complications following total mesorectal excision. Compared with BMI and pelvic index, MFV provides better, although moderate, discrimination for predicting post-operative complications and may serve as a useful imaging biomarker for pre-operative risk stratification. Incorporation of MFV into multivariable prediction models may improve individualized surgical planning and perioperative risk assessment.

Over the past several decades, advances in basic and clinical research have increasingly established cancer-induced cachexia as a distinct pathophysiological syndrome that warrants targeted therapeutic approaches alongside conventional anticancer treatments. Despite its high prevalence and substantial impact on morbidity, mortality, and quality of life, the condition remains underrecognized and inadequately managed in clinical practice. Correspondingly, scientific activity in the field has expanded rapidly, spanning molecular mechanisms, clinical characterization, and emerging interventional strategies.

This bibliometric analysis aims to provide a comprehensive, quantitative overview of evolving research in cancer-induced cachexia over the past 25 years. We conducted a bibliometric analysis of cancer cachexia research published between 2001 and 2025 using the Web of Science Core Collection. A total of 5775 English-language primary research articles were retrieved using the search terms "cancer AND cachexia," and including papers in English of the types articles, letters, and proceedings papers. Data were analyzed using the Bibliometrix R package and its web interface, BiblioShiny, to assess publication trends, author productivity, collaboration networks, and keyword co-occurrence. Additional visualizations were generated using the R programming language and AI-guided analyses to explore trends and bursts in the evolution of cachexia research.

Cancer cachexia publications increased at an annual rate of 6.7%, exceeding the overall growth rate of scientific literature. In terms of number of papers and citation indices, the Journal of Cachexia, Sarcopenia and Muscle is the dominant journal in the field. Research is characterized by high levels of international collaboration, though research networks remain geographically clustered. Keywords were analyzed using co-occurrence networks to reveal specific connections and clusters of research topics. Trend analyses of keywords showed the progression of research in the areas of metabolism and the role of inflammatory mediators. Burst analysis revealed research "hotspots" over the last 25 years including studies of specific interventions such as immunotherapy, gastrointestinal cancers, and metabolic dysregulation.

Cancer cachexia research has expanded significantly over the past two decades but remains limited in scale and fragmented across geographic and disciplinary boundaries. A shift toward investigating biological mechanisms and therapeutics indicates a maturing field with growing translational potential. Growing trends and recent research bursts in immune function and inflammation suggest an important role of these areas in further therapeutic development. Continued integration of clinical, nutritional, and molecular research will be essential to advance effective interventions. This bibliometric analysis offers a data-driven foundation to inform future research priorities and collaboration strategies in cancer-induced cachexia.

We examined whether chromobox protein 5 (CBX5) contributes to temozolomide (TMZ) resistance in O⁶-methylguanine-DNA methyltransferase (MGMT)-negative glioblastoma (GBM) and whether it is regulated by methyltransferase-like 3 (METTL3)-dependent N⁶-methyladenosine (m⁶A) and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2).

Public datasets, clinical specimens, MGMT-negative cells, and subcutaneous xenografts were examined using functional, mechanistic, and rescue assays.

In the CGGA693 cohort of the Chinese Glioma Genome Atlas, higher CBX5 expression remained associated with shorter survival after multivariable adjustment (hazard ratio 1.178, 95% confidence interval 1.050-1.322; p = 0.005). CBX5 depletion increased TMZ sensitivity, apoptosis, and DNA damage, reduced ATM phosphorylation and RAD51 abundance, and restricted TMZ-treated xenograft growth; overexpression produced reciprocal effects in vitro. METTL3 depletion reduced CBX5 expression, mRNA stability, m⁶A enrichment, and wild-type reporter activity but did not significantly affect the m⁶A motif-mutant reporter. IGF2BP2 depletion reduced CBX5 protein and mRNA stability, whereas RNA immunoprecipitation supported an IGF2BP2-CBX5 mRNA association. CBX5 re-expression partially reversed METTL3 depletion-induced effects on viability and DNA damage.

METTL3-dependent m⁶A modification and IGF2BP2-associated stabilization help maintain CBX5 expression, contributing to TMZ resistance and ATM-RAD51-associated signaling in MGMT-negative GBM models.

Gallbladder cancer (GBC) is a biologically complex malignancy arising from the epithelial lining of the gallbladder, with adenocarcinoma constituting the major histological subtype. Early detection is challenging because of vague clinical manifestations and the organ's deep-seated anatomical location, resulting in diagnosis at advanced stages and limited treatment options. Consequently, patients often experience poor prognosis with low 5-year survival rates. Clinical and translational studies have demonstrated marked biological heterogeneity in GBC, primarily driven by diverse molecular alterations that fuel tumor initiation and progression.

In the present study, we investigated recurrently mutated genes in GBC using The Cancer Genome Atlas (TCGA) and Catalogue of Somatic Mutations in Cancer (COSMIC) gallbladder cohorts, focusing on genes with a mutation frequency above a pre-specified threshold (≥ 5% in at least one dataset). We then cross-referenced these genes with published literature till date in GBC and other solid tumors where the same variants have been functionally characterized as loss-of-function or gain-of-function. "Likely loss of function" was assigned only when mutations were annotated in OncoKB/COSMIC as truncating/nonsense or as missense variants with experimental or strong computational evidence of functional impairment.

Evaluation and the functional impact of prominent mutations viz. TP53, SMAD4, PIK3CA, CDKN2A, ARID1A, ARID2, KRAS, ELF3, ERBB3, ERBB2, STK11, and CTNNB1 on key cellular signaling pathways that regulate GBC initiation and progression. These alterations influence various oncogenic mechanisms, including cell proliferation, survival, apoptosis evasion, and metastatic potential, by disrupting pathways. By comparing the mutational patterns observed in GBC with those reported in other malignancies sharing analogous molecular signatures, we delineate potential therapeutic vulnerabilities.

Mutation-guided therapeutic approaches hold great promise for advancing precision medicine in GBC. By tailoring treatments to the specific molecular alterations driving tumor development, this could pave the way for more effective interventions and improved patient outcomes in a disease long constrained by limited therapeutic options.